纯度 | >90%SDS-PAGE. |
种属 | Human |
靶点 | RIPPLY2 |
Uniprot No | Q5TAB7 |
内毒素 | < 0.01EU/μg |
表达宿主 | E.coli |
表达区间 | 1-128 aa |
活性数据 | MENAGGAEGT ESGAAACAAT DGPTRRAGAD SGYAGFWRPW VDAGGKKEEE TPNHAAEAMP DGPGMTAASG KLYQFRHPVR LFWPKSKCYD YLYQEAEALL KNFPIQATIS FYEDSDSEDE IEDLTCEN |
分子量 | 13.9 kDa |
蛋白标签 | His tag N-Terminus |
缓冲液 | PBS, pH7.4, containing 0.01% SKL, 1mM DTT, 5% Trehalose and Proclin300. |
稳定性 & 储存条件 | Lyophilized protein should be stored at ≤ -20°C, stable for one year after receipt. Reconstituted protein solution can be stored at 2-8°C for 2-7 days. Aliquots of reconstituted samples are stable at ≤ -20°C for 3 months. |
复溶 | Always centrifuge tubes before opening.Do not mix by vortex or pipetting. It is not recommended to reconstitute to a concentration less than 100μg/ml. Dissolve the lyophilized protein in distilled water. Please aliquot the reconstituted solution to minimize freeze-thaw cycles. |
以下是关于重组人RIPPLY2蛋白的示例性参考文献(注:内容为模拟概括,建议通过学术数据库核对真实文献):
1. **文献名称**:*Ripply2-mediated suppression of Wnt/β-catenin signaling is essential for somitogenesis*
**作者**:Sasaki, N., et al.
**摘要**:研究揭示了RIPPLY2通过抑制Wnt/β-catenin信号通路调控体节分节的分子机制,重组RIPPLY2蛋白的体外实验表明其直接结合转录因子Tcf/Lef,阻遏靶基因表达。
2. **文献名称**:*Functional interaction between Ripply2 and Mesp2 in the vertebrate segmentation clock*
**作者**:Takahashi, Y., et al.
**摘要**:文章提出RIPPLY2与MESP2形成负反馈环路,重组人RIPPLY2蛋白的过表达实验显示其通过抑制Notch信号通路精确调控体节边界的形成。
3. **文献名称**:*Mutations in RIPPLY2 cause congenital scoliosis by disrupting somitogenesis*
**作者**:Chen, H., et al.
**摘要**:该研究结合临床突变分析,发现RIPPLY2蛋白的功能缺失突变会破坏其与MESP2的相互作用,重组突变体蛋白实验证实其对体节分节的关键作用。
4. **文献名称**:*Ripply2 as a coordinator of BMP signaling during skeletal development*
**作者**:Hitachi, K., et al.
**摘要**:通过体外重组RIPPLY2蛋白实验,证明其通过调控BMP-Smad信号通路影响中胚层细胞分化,为骨骼发育异常提供分子机制解释。
如需具体文献,建议通过PubMed或Google Scholar以“Ripply2 protein”“somitogenesis”“recombinant human RIPPLY2”为关键词检索。
**Background of RIPPLY2 Protein**
The RIPPLY2 protein (also known as Ripply2 or Ribeye-related protein 2) is a member of the Ripply family of transcriptional regulators, primarily studied for its role in vertebrate embryonic development. It is encoded by the *RIPPLY2* gene in humans and shares homology with proteins across species, including zebrafish (*ripply2*) and mice (*Ripply2*). RIPPLY2 is critically involved in somitogenesis—the process of segmenting the embryonic mesoderm into somites, which give rise to vertebral columns, muscles, and other tissues.
Functionally, RIPPLY2 acts as a transcriptional co-repressor, interacting with segmentation clock components like MESP2 and TBX6 to regulate the periodic formation of somites. It modulates Notch and Wnt signaling pathways, ensuring proper spatial-temporal coordination during somitogenesis. Studies in model organisms, such as zebrafish and mice, highlight its role in establishing rostral-caudal polarity within somites and suppressing segmentation defects.
Dysregulation of RIPPLY2 is linked to congenital vertebral malformations, including Klippel-Feil syndrome and congenital scoliosis. Its expression is tightly regulated by retinoic acid signaling and other morphogens, emphasizing its sensitivity to developmental cues. Recent research also explores its potential as a biomarker for cell differentiation in stem cell models.
Despite progress, mechanisms underlying RIPPLY2's interactions with partner proteins (e.g., SALL1/SALL4) remain under investigation. Its dual role in both promoting and repressing transcriptional targets underscores its complexity in developmental biology, making it a key focus for understanding congenital disorders and tissue patterning.
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